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. 2022 Jun 3;23(11):6270. doi: 10.3390/ijms23116270

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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(A) Activated transforming growth factor (TGF)-β type I receptor (TβRI) phosphorylates COOH-tail serine residues of Smad3. Phosphorylated Smad3C translocates with Smad4 to suppress cell growth, stimulating the p21^waf1 promoter. (B) Pro-inflammatory cytokines (CK) such as tumor necrosis factor (TNF)-α activate c-Jun N-terminal kinase (JNK) or Ras signaling to phosphorylate the linker region of Smad3. Linker-phosphorylated Smad3 (pSmad3L) translocates with Smad4 to the nucleus and up-regulates c-Myc, stimulating cell proliferation as well as plasminogen activator inhibiter type 1 (PAI-1), promoting cell invasion and migration.